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Acquired immunodeficiency syndrome (AIDS) of the abdominal organs: Imaging features
Acquired Immunodeficiency Syndrome (AIDS) of the Abdominal Organs: Imaging Features Richard M. Gore, Frank H. Miller, and Vahid Yaghmai The liver, spleen, biliary tract, pancreas, and kidneys are commonly affected by opportunistic infection, malignancy, and inflammatory disorders during the course of human immunodeficiency virus (HIV) infection. Clinical manifestations of solid abdominal visceral involvement are protean and usually nonspecific, but it is important to establish a specific diagnosis promptly in these often critically ill patients. This presentation reviews the cross-sectional imaging spectrum of HIV-associated lesions of these organs. Copyright © 1998 by W.B. Saunders Company
WITH human immunodeficiency p ATIENTS virus (HIV)-associated hepatobiliary (Tables 1, 2), pancreatic, splenic, and renal (Table 3) involvement present with a variety of clinical findings: hepatomegaly (66%), splenomegaly (20%), abnormal liver function tests (80%), pancreatic and renal dysfunction, right or left upper quadrant abdominal pain, jaundice, and constitutional symptoms such as fever and malaise. 1-~2 History, physical examination, and liver and renal function tests are usually nonspecific. Although marked elevation of the serum alkaline phosphatase levels suggests either biliary tract disease or diffuse hepatic infiltration by mycobacterial infection or lymphoma, elevations in serum ALT or AST do not correlate with a specific etiology.13 Abnormal renal function may be due to HIV nephropathy or to hydronephrosis caused by obstructing retroperitoneal adenopathy. 14 Because of the limitations of clinical and laboratory examinations, CT and sonography are often obtained to clarify the clinical situation and establish a specific diagnosis. These cross-sectional imaging studies will identify focal hepatic, splenic, renal and/or pancreatic masses, biliary dilatation, or evidence of non-HIV-related diseases such as cholelithiasis or choledocholithiasis. 15 The results of these studies may prompt further procedures, such as endoscopic retrograde cholangiopancreatography (ERCP), in the case of biliary dilatation, or imaging-directed percutaneous biopsy when a focal hepatic, splenic, pancreatic, or renal mass is detected. 16 When these biopsies are taken, special stains and cultures for mycobacterial, mycotic, and viral organisms should be performed in addition to cytological evaluation. (The subject of acute abdominal disease in HIV-positive patients is covered in detail in another article in this issue.)
NEOPLASMS
The opportunistic neoplasms Kaposi's sarcoma (KS) and non-Hodgkin's lymphoma involve the liver and spleen in approximately 15% of patients with AIDS. 17 They are seldom seen alone, but are usually part of multisystemic involvement. KS is an AIDS-defining illness and usually occurs early in the disease course. AIDS-related lymphoma (ARL) typically develops when there is profound imrnunosuppression (CD4 lymphocyte count < 50 ram3). TM Although many patients with AIDS have serological evidence of prior hepatitis B and C exposure, an increased incidence of hepatomas has not been reported. 18,19 Biliary obstruction due to ARL or KS usually results from extrinsic compression by enlarged lymph nodes or direct hepatic involvement. Primary biliary lymphoma or KS is rare.18,19 Renal cell carcinomas have been reported in patients with AIDS and have been attributed to the patient's immunodeficient state. Adenopathy resulting from ARL and KS can cause hydronephrosis.20-22
Kaposi's Sarcoma Kaposi's sarcoma is the most common neoplasm in patients with AIDS. This lesion is a purple nodule macroscopically that microscopically consists of irregularly dilated vascular spaces coated with swollen endothelial cells. 23Nearly one third of patients with cutaneous Kaposi's sarcoma will have hepatic involvement, but this is usually asymptomFrom the Department of Radiology, Northwestern University Medical School, Chicago, IL. Address reprint requests to Richard M. Gore, MD, Department of Radiology, Evanston Hospital, Northwestern University, 2650 Ridge Ave, Evanston, 1L 60201. Copyright © 1998 by W.B. Saunders Company 0887-2171/98/1902-000658. 00/0
Seminars in Ultrasound, CT, andMRI, Vo119, No 2 (April), 1998: pp 175-189
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176 Table 1. Hepatic and Splenic Parenchymal Diseases Associated With HIV Infection
Infection Bacterial Salmonella Rochalimaea Mycobacterial M tuberculosis M avium complex M xenopi Viral Cytomegalovirus Hepatitis B, C and D Herpesvirus Adenovirus HIV Fungal Candida Cryptococcus Histoplasma Aspergillus Coccidia Sporothrix Protozoal Pneumocystis Cryptosporidia Microsporidia Leishmania Toxoplasma
Neoplasms Non-Hodgkin's lymphoma Kaposi's sarcoma Metastatic cancer of the anal canal Drug-related Trimethoprim-sulfamethoxazole Ketoconazole Isoniazid Rifampin Zidovudine Pentamidine Diphenylhydantoin Prochlorperazine Didanosine Fluconazole Oxacillin Dideoxyinosine
atic and detected only at postmortem.24The diagnosis is usually made when cutaneous or nodal disease is discovered. Hepatic involvement typically causes only mildly elevated serum alkaline phosphatase levels.2 Detection of KS on imaging studies is difficult because the tumor spreads via microscopic perivascular infiltration. Although specific lesions are Table 2, Opportunistic Infections and Neoplasms Involving the Liver
% of Cases Infection Cytomegalovirus MAC Unspecified acid-fast bacilli Cryptococcus neoformans Histoplasma capsulatum Mycobacteria tuberculosis Candida albicans Neoplasms Kaposi's sarcoma Non-Hodgkin's lymphoma
14 11 5.9 2.0 1.2 1,2 0,6 8.6 1,5
Modified and reprinted by permission of the publisher from Bonacini M: Hepatobiliary Complications in Patients with Human Immunodeficiency Virus Infection. Am J Med 92:40441 I. Copyright 1997 by Excerpta Medica Inc.
Table 3. Renal Lesions Associated With HIV Infection
Disseminated infections Cytomegalovirus Mycobacterium tuberculosis Mycobacterium avium complex Cryptococcus Candida albicans Pneumocystis carinii Histoplasmosis HIV
Neoplasms Kaposi's sarcoma Lymphoma Renal cell carcinoma
Acute tubular necrosis Toxic Ischemic
Glomerular lesions Focal and segmental glomerulosclerosis (HIVassociated nephropathy) Mesangial proliferative glomerulonephritis Minimal change disease Membranoproliferative glomerulonephritis Membranous glomerulonephritis Acute postinfectious glomerulonephritis Vascular lesions Hemolytic-uremic syndrome Infarcts Renal cortical necrosis Vasculitis Allergic interstitial nephritis Drug-induced
rarely identified sonographically, hepatosplenomegaly may be present and small hyperechoic periportal and splenic nodules may be visualized causing increased periportal echogenicitye5 (Fig 1A). CT scans occasionally demonstrate low attenuation periportal lesions (Figs 1B, 2A) on noncontrast scans, which subsequently show enhancement on delayed, post-contrast scans. 25-28This finding is nonspecific. Distinctive CT features that indicate the diagnosis include the presence of normal or mildly enlarged lymph nodes that have high density approaching the attenuation of enhancing blood vessels due to the hypervascularity of the tumor26,27 (Fig 2B). They are usually observed in the groin but can be retroperitoneal, axillary, or pelvic in location.27 Skin nodules and nodular metastases to the hollow viscera and lung may also be seen. Renal involvement is usually microscopic and, consequently, found at autopsy rather than on imaging studies. If KS involves and enlarges the retroperitoneal lymph nodes, secondary obstructive uropathy may develop. 29,30
Lymphoma Non-Hodgkin's lymphoma is the second most common malignancy involving the liver, spleen, and kidneys in patients with AIDS.27 The frequency of non-Hodgkin's lymphoma is much higher in patients with AIDS than the general population and the disease course also differs. AIDS-related lym-
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phomas (ARLs) generally are B cell type centroblastic, lymphoblastic, or immunoblastic and are relatively aggressive, undifferentiated forms of lymphoma. 17 ARL tends to have a more advanced grade, greater extranodal disease, and a worse prognosis compared with lymphomas occurring in patients without AIDS. Their poor prognosis is also worsened by associated infections. On crosssectional imaging, ARLs present with hepatosplenomegaly, nephromegaly, and focal lesions. These lesions may vary in size and number: from a large isolated mass to innumerable tiny lesions (Fig 3). Focal lesions can also cause biliary dilatation. Focal hepatic lesions are observed much more commonly on ultrasound (45%) and CT (29%) in ARL when compared with the 5% to 10% incidence of focal abnormalities observed in sporadically occurring lymphoma. 31-34 Focal splenic le-
Fig 2. Kaposi's sarcoma in a 28-year-old man with AIDS. (A) CT scan demonstrates mesenteric and retroperitoneal lymphadenopathy with low density masses extending into the gastrohepatic ligament (black arrow) and portal veins (white open arrow). Hypodense splenic lesions (white arrow) are also identified. (B) This patient also has enlarged, contrastenhancing groin lymph nodes characteristic of adenopathy due to Kaposi's sarcoma (white arrows}.
sions are observed in 7% of AIDS patients and splenomegaly in 40% of cases. 31-34 Six to twelve percent of patients with ARL have renal involvement on imaging studies, which usually manifests as bilateral, discrete parenchymal masses (Fig 4), rather than the diffuse nephromegaly that typifies renal lymphoma in non-AIDS patients. Extensive retroperitoneal and/or mesenteric adenopathy is observed in 56% of ARL. 3~ These nodes usually have soft tissue density, but can occasionally show central necrosis. 35-37 They can also obstruct the renal collecting systems and ureters 37-39(Fig 5). INFECTIONS Fig 1. Kaposi's sarcoma in a 36-year-old man with AIDS. (A) Oblique sonogram demonstrates a periportal hyperechoic liver lesion (calipers) and echogenic periportal bands (arrows). Lymphoma and mycobacterial lesions of the liver tend to be hypoechoic while Kaposi's sarcoma lesions tend to be hyperechoic. (B) Post-contrast CT scan shows low attenuation periportal changes.
HIV infection causes progressive depletion of T-helper lymphocytes that play a pivotal role in the regulation of the immune system. As a result, AIDS patients are extraordinarily susceptible to opportunistic fungal, viral, protozoan, and mycobacterial
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infections.4° Unfortunately, these patients may reveal few systemic signs of infection and laboratory values may be misleading because there may be little fever or associated leukocytosis. Accordingly, cross-sectional imaging will occasionally reveal large abscesses that are clinically occult. Hepatic, splenic, biliary tract, pancreatic, and renal infections may develop during any stage of HIV disease, from the otherwise asymptomatic state to end-stage immunodeficiency. The specific organism infecting a given patient is determined by the degree o f immunosuppression. Most bacterial diseases, including Mycobacterium tuberculosis (MTB), are seen at early or intermediate stages of immunocompromise, when the CD4 lymphocyte count is 200 to 750 mm 3. Protozoan and fungal infections, such as cryptosporidiosis and Pneumocystis carinii (PC), occur when the CD4 lymphocyte count is less than 200 mm 3. Mycobacterium avium intracellular complex (MAC) and cytomegalovirus (CMV) infections almost always develop in the setting of profound immunosuppression (CD4 lymphocyte count < 60 mm3).4°
Fig 4. A 33-year-old woman with disseminated extranodal AIDS-related lymphoma. (A) Multiple low attenuation liver masses are identified (arrows). (B) Low attenuation renal lesions (black arrows) and retroperitonea! lymphadenopathy (open arrow) are seen. Renal biopsy demonstrated nonHodgkin's lymphoma in this patient.
Mycobacterium Avium Complex
Fig 3. A 42-year-old man with AIDS-related non-Hodgkin's lymphoma. (A) Multiple small hypodense liver masses are present. (B) Following chemotherapy, the liver lesions resolved.
Disseminated MAC infection is insidious, with a relatively late presentation, producing fever, anorexia, adenopathy, hepatosplenomegaly, and elevation of liver function tests.4~43 The most common abdominal sonographic and CT finding is lymphadenopathy44,45 (Fig 6). Radiological evidence of parenchymal involvement is often absent in spite of significant pathological involvement; focal lesions occur much more often in MTB than MAC. Perhaps the greater attenuation of the host immune status accounts for the absence of focal masses in MAC. Histologically, MAC causes multiple noncaseating grannlomas within the lobular parenchyma and portal tracts of the liver.46 MAC may present as multiple hypodense lesions on CT due to granuloma formation.4~ Sonographically, multiple tiny echogenic foci in the liver and
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Fig 5. AIDS-related lymphoma in a 38-year-old man. (A) Retroperitoneal adenopathy and direct renal invasion causes hydronephrosis of the left kidney. (B) The left psoas muscle is also involved.
kidneys similar to extrapulmonary PC infection have been reported. 47,48Most commonly, however, only hepatosplenomegaly is observed on imaging studies. A high index of suspicion is required when processing biopsy specimens. They should be routinely stained for acid-fast bacilli and cultured for MAC, because caseating granulomatous reaction may be absent in patients with AIDS. 49 In the clinical setting of profound immunosuppression, the presumptive diagnosis of MAC can be made without biopsy if CT demonstrates focal hepatic, splenic, or renal (Fig 7) lesions associated with enlarged soft tissue density retroperitoneal or mesenteric lymph nodes (Fig 8) and focal jejunal thickening. 3°
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Fig 6. Hepatosplenomegaly associated with Mycobacterium avium complex. (A) CT scan shows mild hepatosplenomegaly associated with mesenteric and retroperitoneal lymphadenopathy. (B) A scan obtained several cm lower reveals adenopathy and focal mural thickening of the jejunum (arrow) and thickening of the gallbladder wall.
other evidence of AIDS and involve the liver, spleen, pancreas, and kidneys without pulmonary involvement.51 Less typical presentations are becoming more prevalent, and extrapulmonary in-
Mycobacterium Tuberculosis (MTB) After decades of decreasing incidence, a resurgence of MTB infection has accompanied the AIDS epidemic. 5° MTB infection may develop before
Fig 7. M),cobacterium avium complex renal abscess in a 40-year-old man with AIDS, Kaposi's sarcoma, and CMV infection of the esophagus, colon, and retina. Biopsy of this low density left renal mass demonstrated MAC.
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Fig 8. Retroperitoneal adenopathy associated with Mycobacterium avium complex. This organism was cultured after percutaneous biopsy of the 2 cm lymph node (arrow),
volvement is identified in up to 70% of AIDS patients with MTB including involvement of the liver, spleen, lymph nodes, central nervous system, bone, gastrointestinal tract, kidney, and soft tissues. 52 The liver is less commonly involved with MTB than MAC. Unlike MAC, MTB infection may occur before patients are significantly immunosuppressed. On CT, MTB presents with multifocal lesions in the liver, spleen (Fig 9), kidney (Fig 10), and pancreas often associated with enlarged, retroperitoneal and mesenteric lymph nodes that usually have central necrosis.41 Concomitant segmental ileocecal wall thickening may also be observed on CT. Hepatosplenomegaly is more impressive in MAC than in MTB. Low density lymph nodes are observed in 93% of patients with MTB but in only 14% of patients with MAC. 41
Fig 9. Mycobacterium tuberculosissplenic abscesses. Multiple hypodense lesions are seen within the spleen,
Fig 10. Mycobacterium tuberculosis renal abscess. (A) Longitudinal sonogram demonstrates an inhomogeneous mass (cursors) at the lower pole of the left kidney, (B) CT demonstrates a low density mass with a thick wall in the same region,
giF~ses
HIV infection is associated with disseminated hepatitis B and C viruses, CMV, herpes simplex virus, and Epstein-Barr virus due to similar modes of transmission. With acute hepatitis, sonography may demonstrate hepatomegaly associated with decreased liver echogenicity and prominent portal triads and mural thickening of the gallbladder. CT usually shows only hepatomegaly. Hepatitis B and C viruses can cause acute or chronic active hepatitis and ultimately postnecrotic cirrhosis. On crosssectional imaging, postnecrotic cirrhosis manifests as a nodular hepatic contour, enlargement of the caudate lobe and lateral segment of the left lobe, prominence of the fissures, regenerating nodules, and atrophy of the right and quadrate lobes. Sono-
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graphically, there is increased reflectivity of the fibrous tissue and a concomitant loss of definition of the portal vein walls associated with a generalized coarse, irregular, and heterogeneous echo architecture.53 CMV infection is common in patients with AIDS, seen in up to two thirds of autopsies. CMV may affect any part of the GI tract, generally presenting with ulcers of the esophagus, stomach, and/or colon, s4,55 Hepatic, renal, and pancreatic involvement is observed less frequently. Coinfection with cryptosporidium and Candida albicans is common. CMV involves the liver in up to 44% of AIDS patients at autopsy, but generally is clinically silent unlike biliary, gastrointestinal, or pulmonary infection)4,55 CMV infection may manifest with multiple echogenic liver lesions sonographically and multiple low attenuation lesions on CT (Fig 11). Hepatic or renal infection by CMV does not significantly alter patient prognosis) 6
Bacterial Abscesses All AIDS patients, but particularly those who are intravenous drug abusers, are prone to develop septic emboli and abscesses from a variety of bacteria, most often Staphylococcus aureus. The lungs, liver, spleen (Fig 12), and kidneys (Fig 13) may also be involved due to hematogenous disseminationY ,58 Multiple organisms are often cultured from these abscesses.
Fungal Infections The liver and spleen are often infected in AIDS patients with disseminated Candida albicans, 59 Cryptococcus neoformans, HistopIasma capsularum, and Coccidioides immitis organisms. Candidiasis can cause hepatic, splenic (Fig 14), pancreatic, and renal microabscesses, especially in intravenous drug abusers. The diagnosis of candidiasis can be difficult because the clinical and radiological presentation is nonspecific, and this organism may be difficult to culture following biopsy.59,6° Additionally, blood cultures are positive in only 50% of patients. Candida microabscesses typically appear as multiple small hypoechoic lesions on sonography or hypodense lesions on CT scans, best seen following intravenous contrast material injection. 6°,61
Pneumocystis Carinii Extrapulmonary PC infection is occurring more frequently in AIDS patients due to their longer life
Fig 11. Focal hepatic lesions associated with CMV infection. (A) CT shows multiple hypodense liver masses. (B) These lesions are echogenic on ultrasound,
span and the introduction of prophylactic aerosolized pentamidine.62 Although therapy produces drug levels sufficient to prevent pulmonary infection, systemic distribution is inadequate, encouraging extrapulmonic disease spread to the liver, spleen, kidneys, lymph nodes, bone marrow and, less often, to the adrenal glands, retina, thyroid and parathyroid glands, gallbladder, and pancreas. Pneumocystis carinii pneumonia spreads both hematogeneously and lymphogeneously. Fortunately, extrapulmonic spread occurs in fewer than 1% of patients. Disseminated disease is usually a premorbid event unless systemic treatment is provided, only a solitary extrapulmonary site is involved, or if there is no concurrent active pulmonary infection. Sonography of the liver, spleen, and kidneys
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Fig 12. Pyogenic and protozoan abscesses in a 34-year-old febrile man with AIDS and splenic abscesses, CT demonstrates several hypodense splenic lesions one of which has peripheral calcification. Percutaneous aspiration revealed Pneumocystis carinii, Klebsiella, and E coli,
may show small hypoechoic masses or multiple tiny echogenic foci without shadowing 62-64 (Fig 15). The echogenic loci are due to calcifications or granulomas. CT scans may demonstrate hypodense lesions or calcifications of the liver, spleen and kidneys 62-65 (Fig 16). Associated findings include punctate calcifications of the adrenal glands and lymph nodes. A history of PC pneumonia, aerosolized pentamidine prophylaxis, and progressive calcification of the liver, spleen, and other organs is suggestive of extrapulmonary PC infection.62Calcifications within these lesions do not necessarily signify healed, inactive disease as they do in candidiasis and lymphoma. These calcifications were initially believed to be pathognomonic for pneumocystis infection, but have recently been
Fig 13. Bilateral wedge-shaped infarcts due to septic emboll are seen in the kidneys of this AIDS patient with E coil septicemia. Note the splenomegaly,
GORE, MILLER, AND YAGHMAI
Fig 14. Candidiasis in a 33-year-old intravenous drug abuser with AIDS. Splenic involvement manifests as multiple small low attenuation lesions.
described in MAC and cytomegalovirus infection.66,67 AIDS-RELATED CHOLANGITIS
Although hepatic parenchymal involvement with opportunistic infection and malignancy has been well described, the biliary tract sequelae of HIV infection are less well appreciated. Four different patterns of HIV-related cholangiopathy have been reported: 1. Papillary stenosis in which there is dilatation of bile ducts and delayed drainage of contrast into the duodenum. 2. Sclerosing cholangitis characterized by focal strictures and dilatations of the intra- and/or extrahepatic bile ducts. 3. Combined papillary stenosis and intra- and/or extrahepatic sclerosing cholangitis. 4. Long extrahepatic bile duct strictures with lengths exceeding 1 to 2 cm. Biliary tract infections by several organisms, but especially CMV and cryptosporidium, have been implicated in the development of AIDS-related cholangitis but not directly demonstrated as cansative. 2,68,69Other associated infections include MAC, Microsporidium, and Isospora. 58,7° Direct involvement by HIV infection has also been postulated as causative. CMV-associated acalculous cholecystitis has been described, but does not appear to be associated with HIV cholangiopathy, as the two are rarely observed in the same patient. 71 Pathologically, there is inflammation and edema of the gallbladder wall and mucosal ulceration. CMV inclusion bodies characteristically are located near mucosal ulcers.
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Fig 15. AIDS-related Pneumocystis carinfi infection in a 27-year-old man with prior Pneurnocystis infections who had received prophylactic aerosolized pentamidine. (A) Longitudinal sonogram demonstrates multiple tiny echogenic foci in the liver and right kidney, (B) Multiple tiny echogenic foci are also present on this longitudinal scan of the spleen. (C) Corresponding CT reveals multiple calcifications in the spleen and gastrohepatic ligament, Calcifications are typical of Pneumocystis infection and may be present in both active and resolved infections.
Cryptosporidiosis infection is present in 6% of all AIDS patients and 21% of those with diarrhea. 72 The identification of biliary cryptosporidium is difficult; currently, there is no effective therapy for the irradiation of this organism. 59,73 Ultrasound, CT scans (Figs 17 through 19), and ERCP are complementary in the diagnosis of AIDS-related cholangiopathy. 74-%Ultrasound findings include dilatation and mural thickening of the gallbladder and common bile ducts as well as pericholecystic fluid. Dilated intrahepatic ducts are
often observed. 74,78 An echogenic nodule may be seen at the distal end of the common bile duct representing an edematous papilla of Vater. Gallbladder dilatation and sludge are also commonly found in AIDS patients. On CT, inflammation of the gallbladder or biliary tree is manifested by mural thickening and/or abnormal contrast enhancement. The cholangiographic signs of beading, pruning, and nodular mural thickening can also be observed. Patients with AIDS often have asymptomatic gallbladder wall thickening that does not
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require treatment. The exact cause is unknown and may relate to hepatic dysfunction, hepatitis, hypoproteinemia, or opportunistic infections (typically CMV and cryptosporidium) that may induce acalculous cholecystitis. Reversible symptomatic gallbladder wall thickening has been described during infusion of interleukin-2 therapy. 74-v9 Cholangiography is more sensitive and specific than ultrasound and CT in depicting the shagginess and mural irregularity of the extrahepatic ducts that result from exuberant periductal inflammation, focal mucosal ulcers, and interstitial edema found in AIDS-related cholangitis. In addition, therapeutic procedures such as sphincterotomy, especially in patients with papillary stenosis, may provide temporary symptomatic relief. However, ERCP is invasive and can cause pancreatitis.
Fig 17. Mural thickening of the gallbladder in a 43-year-old AIDS patient with elevated liver function tests and Cryptosporidiurn infection. (A) Longitudinal sonogram shows marked mural thickening of the gallbladder (arrows). (B) CT scan shows low density wall thickening with enhancing mucosa causing "pseudogallstone" appearance (arrow). Note the periportal lucency, which is usually caused by secondary periportal edema related to lymphadenitis, hepatitis, or malnutrition. Mild retroperitoneal adenopathy is also seen.
PARENCHYMAL LIVER DISEASE
Fig 16. Extrapulmonary Pneumocystis carinfi infection. (A) Transverse sonogram demonstrates echogenic reflectors in the right kidney secondary to calcifications. (B) Non-contrast CT scan shows multiple renal calcifications. When extrapulmonary Pneumocystis is suspected, non-contrast images should be obtained.
A wide variety of disorders (Tables 1, 2) associated with HIV infection and AIDS can affect the liver. Although most of these represent opportunistic infections, ARL, KS, and hepatocellular injury from drugs used in the treatment of AIDS also must be considered. Additionally, there may be coexisting liver disease unrelated to HIV infection such as chronic viral hepatitis or liver injury from alcohol or drug abuse. Serological markers for concurrent hepatitis B virus infection are present in 90% of patients with AIDS. This concurrent infection does not appear to alter the natural history of HIV infection. Hepatic steatosis is a common postmortem find-
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ing in patients with AIDS. s° The pathogenesis of fatty change is complex and relates to the effects of circulating cytokines such as tumor necrosis factor, interleukin- 1, and interferons.Sl Focal fatty infiltration can mimic other mass lesions. Imaging findings of hepatic steatosis are similar to those found in non-AIDS patients. 53 On CT, there are diffuse, focal, segmental, or geographic areas of low attenuation in the liver. Sonographically, involved areas show accentuation of echogenic foci resulting from the proliferation of fat-nonfat interfaces. This leads to rapid attenuation of the insonating ultrasound beam. A diffusely echogenic liver can also result from multiple granulomata secondary to infections such as MAC, MTB, cryptococcosis, histoplasmosis, and toxoplasmosis. 82-85Drug toxicity may manifest as hepatic steatosis or as multiple granulomas that also cause an echogenic liver on sonography, sl Bacillary peliosis hepatitis is a recently recog-
Fig 19. Cryptosporidiosis of the bile ducts and small bowel in an HIV-positive 22-year-old man with diarrhea and elevated liver enzyme levels. (A) CT scan shows dilated intrahepatic ducts that have thick enhancing walls. (B) More caudal scan shows mural thickening of the small bowel,
Fig 18. AIDS-induced papillary stenosis due to cryptosporidiosis in a 33-year-old man. (A) Oblique sonogram demonstrates dilatation of the common hepatic duct and mural thickening of the gallbladder {arrows), (B) Transverse sonogram of the pancreas shows dilatation of the common bile duct (large arrow) and pancreatic duct (small arrow),
nized complication of AIDS, found in patients with CD4 lymphocyte counts < 200 per mm 3. It is caused by systemic infection by either Rochalimaea henselae or Rochalimaea quintana, two newly recognized bacteria related to Bartonella species, of the Rickettsiae order. This disorder is associated with cutaneous angiomatous lesions and lytic bone lesions and clinically manifests with fever, chills, sweats, bone pain, and abdominal or right upper quadrant pain. Pathologically, there are dilated vascular lakes that are associated with proliferation of sinusoidal endothelial cells, blebbing of hepatocyte membranes, extravasation of red blood cells, and dilatation of Disse's spaces. 86 The CT findings vary based on the size of the vascular cavities. Small cavities are not visible on cross-sectional imaging studies, whereas larger cavities may have an attenuation similar to blood vessels or appear as hypodense defects. Complications such as liver failure, portal hypertension, and
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hemorrhage from hepatic or splenic rupture may develop, s6.Ss PANCREATIC DISEASES
Pancreatic diseases, although commonly detected at autopsy, often are not recognized during life but can be a source of morbidity in patients with AIDS. 7~ These patients are subject to a variety of pancreatic disorders in addition to those seen in the general population: opportunistic infections, drug-induced inflammation, and neoplasms, s9 Involvement can range from asymptomatic findings detected at autopsy to fulminant pancreatitis leading to death. Gross pathological changes vary from a normal pancreas in some infections and tumors to massive necrosis and abscess formation. Special stains for fungi and mycobacteria and detection of viral inclusions are required for diagnosis following biopsy. Generally, the patients are asymptomatic with involvement of other organs by infections or neoplasms. 9° Reported opportunistic infections that affect the pancreas include CMV (Fig 20), MAC, MTB, Cryptococcus neoformans, Aspergillosis, and candidiasis. 55 Extrapulmonary PC rarely involves the pancreas and may be seen as tiny echogenic foci on ultrasound or calcifications on CT examination. 91 Medications including pentamidine and trimethoprim-sulfamethoxazole, both used to treat PC pneumonia, can cause pancreatitis indistinguishable from other causes. There is a 7% prevalence rate of pancreatic neoplasms in AIDS patients at autopsy, most commonly, Kaposi's sarcoma and lymphoma. The involvement appears to be subclinical and usually is associated with disseminated disease. The radiographic features of pancreatitis and pancreatic abscesses in patients with AIDS are similar to that of the general population. Two caveats should be remembered when using ultrasound. When comparing pancreatic to hepatic parenchymal echogenicity, it should be remembered that the liver is often echogenic in patients with AIDS due to fatty infiltration, so that the normal pancreas may appear relatively hypoechoic, simulating pancreatitis. 53 Similarly, the kidney is not always a reliable internal reference; the parenchyma may be hyperechoic due to HIV-associated nephropathy. HIV NEPHROPATHY
HIV-associated nephropathy can develop in patients with asymptomatic HIV infection, AIDS-
Fig 20. Cytomegalovirus pancreatitis with pseudocysts in a 33-year-old man with AIDS. (A and B) This AIDS patient had a history of complicated pancreatitis with recurrent pseudocysts (P) noted on sonography and CT scan that required drainage. Pancreatic biopsy confirmed characteristic CMV inclusion bodies.
related complex, or AIDS.92 Patients typically have mild hypertension, large kidneys with early and rapidly progressive renal failure with massive proteinuria, hematuria, and azotemia. 93 Renal involvement is more prevalent in AIDS patients with multiple risk factors and intravenous drug abuse than the homosexual population with AIDS. 94,95 The disease is most commonly seen in black males and has an inexorably downhill course with 100% mortality within 6 months after the onset of uremia despite hemodialysis. Focal and segmental glomeru-
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cortical e c h o g e n i c i t y (Fig 21), w h i c h is m o s t likely the result o f the g l o m e r u l o s c l e r o s i s and the dilated renal tubules filled with proteinaceous material. H o w e v e r , a direct correlation b e t w e e n the extent o f renal disease and d e g r e e of e c h o g e n i c i t y does not exist.96, 97 The m a j o r C T findings in H I V nephropathy include n e p h r o m e g a l y due to p a r e n c h y m a l inflammation and edema, increased attenuation o f the m e d u l l a on non-contrast scans, and a striated n e p h r o g r a m f o l l o w i n g contrast administration due to the dilated tubules filled with proteinaceous material. 9~ SUMMARY Fig 21. A 24-year-old male with HIV nephropathy, Longitudinal sonogram demonstrates an enlarged right kidney with increased cortical echogenicity.
losclerosis are the histopathologic hallmarks o f H I V - a s s o c i a t e d nephropathy. T h e r e is m i c r o c y s t i c dilatation o f renal tubules, with the l u m e n filled with pale-staining casts and n u m e r o u s protein absorption droplets. T h e sonographic correlates o f this p a t h o l o g y are n e p h r o m e g a l y and increased
Hepatic, splenic, biliary tract, pancreatic, and renal c o n s e q u e n c e s o f H I V disease are diverse. S o m e are unique and specifically attributable to H I V infection, whereas others are coincidental, reflecting the nature and severity o f the underlying primary illness. As patients with A I D S are living longer, solid a b d o m i n a l visceral i n v o l v e m e n t is b e c o m i n g m o r e c o m m o n , and an understanding o f the s p e c t r u m o f H I V - a s s o c i a t e d disease is essential for i m p r o v i n g patient m a n a g e m e n t . 99
REFERENCES
1. Poles MA, Lew EA, Dieterich DJ: Diagnosis and treatment of hepatic disease in patients with HIV. Gastroenterol Clin North Am 26:291-322, 1997 2. Nash JA, Cohen SA: Gallbladder and biliary tract disease in AIDS. Gastroenterol Clin North Am 26:323-336, 1997 3. Cappel MS, Hassan T: Pancreatic disease in AIDS--A review. J Clin Gastroenterol 17:254-263, 1993 4. Cello J: Acquired immune deficiency syndrome-related sclerosing cholangitis. Am J Med 86:539-546, 1989 5. Connolly JO, Weston CE, Hendry BM: HIV-associated renal disease in London hospitals. Q J Med 88:627-634, 1996 6. Vuitton D-A, Chossegros P, Bresson-Hadni S, et al: HIV infection, the liver and biliary tract, Part II: Hepatobiliary complications of AIDS. Gastroenterol Clin Biol 20:281-293, 1996 7. Vuitton D-A, Chossegros E Bresson-Hadni S, et al: HIV infection, the liver and biliary tract, Part I: HBV, HDV, and HCV. Gastroenterol Clin Bio120:269-280, 1996 8. Lefkowitch JH: Pathology of AIDS-related liver disease. Dig Dis 12:321-330, 1994 9. Frassetto L, Schoenfeld PY, Hurnphreys MH: Increasing incidence of human immunodeficiency virus-associated nephropathy at San Francisco General Hospital. Am J Kid Dis 18:655-659, 1991 10. Rao TKS: Human immunodeficiency virus (HIV) associated nephropathy. Annu Rev Med 42:391-401, 1991 11. Rao TKS, Friedman EA, Nicastri AD: The types of renal disease in the acquired immunodeficiency syndrome. N Engl J Med 316:1062-1068, 1987
12. Valeri A, Neusy AJ: Acute and chronic renal disease in hospitalized AIDS patients. Clin Nephrol 35:110-118, 1991 13. Chalasani N, Wilcox CM: Etiology, evaluation, and outcome of jaundice in patients with acquired immunodeficiency syndrome. Hepatology 23:728-733, 1996 14. Bourgoignie JJ, Meneses R, Ortiz C, et al: The clinical spectrum of renal disease associated with human immunodeficiency virus. Am J Kidney Dis 12:131-137, 1988 15. Reeders JWAJ, Megibow AJ, Antonides HR: Radiology of gastrointestinal manifestations of AIDS. In Reeders JWAJ (ed): Diagnostic Imaging of AIDS. New York, NY, Thieme Medical Publishers, 1992, pp 92-123 16. Donnelly LF: CT imaging of immunocompromised children with acute abdominal symptoms. AJR 167:909-913, 1996 17. Levine AM: AIDS-associated malignant lymphoma. Med Clin North Am 76:253-268, 1992 18. Hasan FA, Jeffers LJ, Welsh SW, et al: Hepatic involvement as the primary manifestation of Kaposi's sarcoma in the acquired immunodeficiency syndrome. Am J Gastroenterol 84:1449-1451, 1989 19. Ferrozzi F, Bova D, Campodonico E et al: AIDS-related malignancies: Clinico-pathologic correlation. Eur Radiol 5:477485, 1995 20. Nyberg DA, Federle MP: AIDS-related Kaposi's sarcoma and lymphoma. Semin Roeutgeno122:54-65, 1987 21. Cohan RH, Dunnick NR, Leder RA, Baker ME: Computed tomography of renal lymphoma. J Comput Assist Tomogr 14:933-938, 1990
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22. Townsend RR: CT of AIDS-related lymphoma. AJR 156:969-974, 1991 23. Krown SE: Acquired immunodeficiency syndromeassociated Kaposi's sarcoma. Med Clin North Am 81:471-494, 1997 24. Grendell JH, Cello JP: HIV-associated hepatobiliary disease, in Zakirn D, Boyer TD (eds): Hepatology, 3rd ed. Philadelphia, PA, Saunders, 1996, pp 1699-1706 25. Radin R: HIV infection: Analysis in 259 consecutive patients with abnormal abdominal CT findings. Radiology 197:712-722, 1995 26. Towsend PR, Laing FC, Jeffrey RB, et al: Abdominal lymphoma in AIDS: Evaluation with US. Radiology 171:719724, 1989 27. Hefts BR, Megibow AJ, Birnbanm BA, et al: Highattenuation lymphadenopathy AIDS patients: Significance of findings at CT. Radiology 185:777-781, 1992 28. Vails C, Cafias C, Turell LG, et al: Hepatosplenic AIDS-related Kaposi's sarcoma. Gastrointest Radiol 16:342344, 1991 29. Luburich P, Brn C, Ayuso MC, et al: Hepatic Kaposi's sarcoma in AIDS: US and CT findings. Radiology 175:172-174, 1990 30. Miles BJ, Melser M, Farah R, et al: The urologic manifestations of the acquired immunodeticiency syndrome. J Urol 142:771-773, 1989 31. Radin DR, Esplin JA, Levine AM, Rails PW: MDSrelated non-Hodgkin's lymphoma: Abdominal CT findings in 112 patients. AJR 160:113-1139, 1993 32. Scerpella EG, Villareal AA, Casanova PF, et al: Primary lymphoma at the liver in AIDS. J Clin Gastroenterol 22:51-53, 1996 33. Soyer R Van Beers B, Teillet-Thi6band F, et al: Hodgkin's and non-Hodgkin's hepatic lymphoma: Sonographic findings. Abdom Imaging 18:339-343, 1993 34. Wang C-Y, Snow JL, Su WPD: Lymphoma associated with human immunodeficiency virus infection. Mayo Clin Proc 70:665-672, 1996 35. Siskin GP, Hailer JO, Miller S, et al: AIDS-related lymphoma: Radiologic features in pediatric patients. Radiology 196:63-66, 1995 36. Pombo F, Rodriguez E, Caruncho MV, et al: CT attenuation values and enhancing characteristics of thoracoabdominal lymphomatous adenopathies. J Comput Assist Tomogr 18:5962, 1994 37. Strans DJ: Human immunodifficiency virus-associated lymphomas. Med Clin North Am 81:495-510, 1997 38. Townsend RR, Laing FC, Jeffrey RB, et al: Abdominal lymphoma in AIDS: Evaluation with US. Radiology 171:719724, 1989 39. Nyberg DA, Jeffrey RB, Federle ME et al: AIDS-related lymphomas: Evaluation by abdominal CT. Radiology 159:5963, 1986 40. Schacker T, Collier AC, Hughes J, et al: Clinical and epidemiologic features of primary HIV infection. Arch Intern Med 125:257-264, 1997 41. Rubin SA: Tuberculosis and atypical mycobacterial infections in the 1990s. RadioGraphics 17:1051-1059, 1997 42. Markowitz N, Hansen NI, Hopewell PC, et al: Incidence of tuberculosis in the United States among HIV infected persons. Ann Intern Med 126:123-132, 1997
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43. French AL, Benator DA, Gordin FM: Nontuberculous Mycobacterial infections. Med Clin North Am 81:361-380, 1997 44. Marinelli DL, Albelda SM, Williams TM, et al: Nontuberculous mycobacterial infection in AIDS: Clinical, pathologic, and radiographic features. Radiology 160:77-82, 1986 45. Radin DR: Intra-abdominal Mycobacterium tuberculosis vs. Mycobacterium avium-intracellulare infections in patients with AIDS: Distinction based on CT findings. AJR 156:487-491, 1991 46. Telzak EE: qhaberculosis and human immunodeficiency virus. Med Clin North Am 81:345-360, 1997 47. Falkoff G, Rigsby CM, Rosenfield AT: Partial, combined cortical and medullary nephrocalcinosis: US and CT patterns in AIDS-associated MAI infection. Radiology 162:343-344, 1987 48. Towers MJ, Withers CE, Hamilton PA, et al: Visceral calcification in patients with AIDS may not always be due to Pneumocystis carinii. A JR 156:745-747, 1991 49. Beale TJ, Wetton CWN, Crofton ME: A sonographicpathological correlation of liver biopsies in patients with AIDS. Clin Radio150:761-764, 1995 50. Markowitz N, Hansen NI, Hopewell PC, et al: Incidence of tuberculosis in the United States among HIV-infected persons. Ann Intern Med 126:123-132, 1997 51. Moore RD, Chiasson RE: Natural history of opportunistic disease in an HIV-infected urban clinical cohort. Ann Intern Med 124:663-642, 1996 52. Schacker T, Collier AC, Hughes J, et al: Clinical and epidemiologic features of primary HIV infection. Ann Intern Med 125:257-264, 1996 53. Gore RM: Diffuse liver disease, in Gore RM, Levine MS, Lanfer I (eds): Textbook of Gastrointestinal Radiology. Philadelphia, PA, Saunders, 1994, pp 1968-2018 54. Adolph MD, Bass SN, Lee SK, et al: Cytomegalovirus acalculous cholecystitis in acquired immunodeficiency virus infection. Am J Med 92:404-411, 1992 55. Goodgame RW: Gastrointestinal cytomegalovirus disease. Ann Intern Med 119:924-935, 1993 56. Vieco PT, Rochon L, LisonaA: Multifocal cytomegalovirus-associated hepatic lesions simulating metastases in AIDS. Radiology 176:123-124, 1990 57. Murray JG, Patel MD, Lee S, et al: Microabscesses of the liver and spleen in AIDS: Detection with 5-MHz sonography. Radiology 197:723-727, 1995 58. Heyworth MF: Parasitic diseases in immunocompromised hosts: Cryptosporidiosis, isosporiasis, strongyloidiasis. Gastroenteral Clin North Am 25:691-707, 1996 59. Friedman SL. Hepatobiliary infections in AIDS, in Surwicz C, Owen RS (eds): Gastrointestinal and Hepatic Infections. Philadelphia, PA, Sannders, 1995, pp 391-404 60. Hamper UM, Goldblum LE, Hutchins GM, et al: Renal involvement in AIDS: Sonographic-pathologic correlation. AJR 150:1321-1325, 1988 61. Schaffer RM, Schwartz GE, Becker JA, et al: Renal ultrasound in acquired immunodeficiency syndrome. Radiology 153:511-513, 1984 62. Bernard EM, Sepkowitz KA, Telzak EE, et al: Pneumocystis. Med Clin North Am 76:107-120, 1992 63. Lubat E, Megibow AJ, Balthazar EJ, et al: Extrapulmonary Pneumocystis carinii infection in AIDS: CT findings. Radiology 174:157-160, 1990
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64. Spouge AR, Wilson ST, Gopinath N, et al: Extrapulmonary Pneumocystis carinii in a patient with AIDS: Sonographic findings. AJR 155:76-78, 1990 65. Radin DR, Baker EL, Klatt EC, et al: Visceral and nodal calcification in patients with AIDS-related Pneumocystis carinii infection. AJR 154:27-31, 1990 66. Bray HJ, Lail VJ, Cooperberg PL: Tiny echogenic loci in the liver and kidney in patients with AIDS: not always due to disseminated Pneumocystis carinii. A JR 158:81-82, 1992 67. Witt K, Nielsen TN, Junge J: Dissemination of pneumocysfis carinii in patients with AIDS. Scand J Infect Dis 23:691-695, 1991 68. Benhamou Y, Caumes E, Gerosa Y, et al: AIDS-related cholangiopathy. Dig Dis Sci 38:1113-1118, 1993 69. Reeders JWAJ, Bartelsman JFWM, Huibregtse: AIDSrelated manifestations of the bile duct system: A common finding? Abdom Imag 19:423-424, 1994 70. Wittner M, Tanowitz liB, Weiss LM: Parasitic infections in AIDS patients. Infect Dis Clin North Am 7:569-586, 1993 71. Miller FH, Gore RM, Nemcek A, Fitzgerald SW: Pancreaticobiliary manifestations of AIDS. A JR 166:1-10, 1996 72. Quinn D, Popock N, Freund J, et al: Radionuclide hepatobiliary scanning in patients with AIDS-related sclerosing cholangitis. Clin Nucl Med 18:417-422, 1993 73. Forbes A: Acquired immune deficiency syndrome-related sclerosing cholangitis. Eur J Gastroenterol Hepatol 4:455-459, 1992 74. Texidor HS, Godwin TA, Ramirez EA: Cryptosporidiosis of the biliary tract in AIDS. Radiology 180:51-56, 1991 75. DaSilva F, Boudghene F, Lecomte I, et al: Sonography in AIDS-related cholangitis. AJR 160:1205-1207, 1993 76. RomanoAJ, van Sonnenberg E, Casola G, et al: Gallbladder and bile duct abnormalities in AIDS: Sonographic findings in eight patients. AJR 150:123-127, 1988 77. Chung CJ, Sivit CJ, Rakusan TA, et al: Hepatobiliary abnormalities on sonography in children with HIV infection. J Ultrasound Med 13:205-210, 1994 78. Pantongrag-Brown L, Nelson AM, Brown AE, et al: Gastrointestinal manifestations of acquired immunodeficiency syndrome:radiologic-pathologic correlation. RadioGraphics 15: 1155-1178, 1995 79. Tanowitz HB, Simon D, Wittner M: Gastrointestinal manifestations of AIDS. Med Clin North Am 76:45-62, 1992 80. Bach N, Theise ND, Schaffner F: Hepatic histology in the acquired immunodeficiency syndrome. Semin Liver Dis 12:205212, 1992 81. Fortgang IS, Belitsos PC, Chalsson RE, et al: Hepatomegaly and steatosis in HIV-infected patients receiving nucleoside analog antiretroviral therapy. Am J Gastroenterol 90:14331436, 1995
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82. Wetton CWN, McCarty M, Tomlinson D, et al: Ultrasound findings in hepatic mycobacterial infections in patients with acquired immunodeficiency syndrome (AIDS). Clin Radiol 47:36-38, 1993 83. Jeffrey RB: Abdominal imaging in the immunocompromised patient. Radiol Clin North Am 30:79-596, 1992 84. Townsend RR, Jeffrey RB: Ultrasonography in AIDS. Ultrasound Q 7:293-314, 1989 85. Daar ES, Meyer RD: Bacterial and fungal infection. Med Clin North Am 76:176-204, 1992 86. Mohle-Boetani JC, Koehler JE, Berger TG, et al: Bacillary angiomatosis and bacillary peliosis in patients infected with human immunodeficiency virus: Clinical characteristics in a case-controlled study. Clin Infect Dis 22:794-800, 1996 87. Moore EH, Russell LA, Klein JS, et al: Bacillary angiomatosis in patients with AIDS: Multiorgan imaging findings. Radiology 197:67-72, 1995 88. Wyatt SH, Fishman EK: Hepatic bacillary angiomatosis in a patient with AIDS. Abdom Imaging 18:336-338, 1993 89. Cappell MS: The pancreas in AIDS. Gastroenterol Clin North Am 26:337-366, 1997 90. Farman J, Brunetti J, Baer JW, et al: AIDS-related cholangiopancreatographic changes. Abdominal Imaging 19:417422, 1994 91. Radin DR, Baker EL, Klatt EC, et al: Visceral and nodal calcification in patients with AIDS-related Pneumocystis carinii infection. AJR 154:27-31, 1990 92. Rat TKC: Renal complications in HIV disease. Med Clin North Am 80:1437-1451, 1996 93. Glassock RJ, Cohen AH, Danovitch G, et al: Human immunodeficiency virus (HIV) infection and the kidney. Ann Intern Med 112:35-49, 1990 94. Humphreys MH: Human immunodeficiency virusassociated glomernlosclerosis. Kidney Int 48:311-315, 1995 95. Bargman JM, Wagner C, Cameron R: Renal cortical nephrocalcinosis: A manifestation of extrapulmonary Pneumocystis carinii infection in the acquired immunodeficiency syndrome. Am J Kidney Dis 17:712-715, 1991 96. Kuhlman JE, Browne D, Shermak M, et al: Retroperitoneal and pelvic CT of patients with AIDS: Primary and secondary involvement of the genitourinary tract. RadioGraphics 11:473-483, 1991 97. Kay KJ: Renal diseases in patients with AIDS: Sonographic findings. AJR 159:551-554, 1992 98. Miller FH, Parikh S, Gore RM, et al: Renal manifestations of AIDS. RadioGraphics 13:587-596, 1993 99. Gourevitch MN: The epidemiology of HIV and AIDS. Med Clin North Am 80:1223-1233, 1996
WITH human immunodeficiency p ATIENTS virus (HIV)-associated hepatobiliary (Tables 1, 2), pancreatic, splenic, and renal (Table 3) involvement present with a variety of clinical findings: hepatomegaly (66%), splenomegaly (20%), abnormal liver function tests (80%), pancreatic and renal dysfunction, right or left upper quadrant abdominal pain, jaundice, and constitutional symptoms such as fever and malaise. 1-~2 History, physical examination, and liver and renal function tests are usually nonspecific. Although marked elevation of the serum alkaline phosphatase levels suggests either biliary tract disease or diffuse hepatic infiltration by mycobacterial infection or lymphoma, elevations in serum ALT or AST do not correlate with a specific etiology.13 Abnormal renal function may be due to HIV nephropathy or to hydronephrosis caused by obstructing retroperitoneal adenopathy. 14 Because of the limitations of clinical and laboratory examinations, CT and sonography are often obtained to clarify the clinical situation and establish a specific diagnosis. These cross-sectional imaging studies will identify focal hepatic, splenic, renal and/or pancreatic masses, biliary dilatation, or evidence of non-HIV-related diseases such as cholelithiasis or choledocholithiasis. 15 The results of these studies may prompt further procedures, such as endoscopic retrograde cholangiopancreatography (ERCP), in the case of biliary dilatation, or imaging-directed percutaneous biopsy when a focal hepatic, splenic, pancreatic, or renal mass is detected. 16 When these biopsies are taken, special stains and cultures for mycobacterial, mycotic, and viral organisms should be performed in addition to cytological evaluation. (The subject of acute abdominal disease in HIV-positive patients is covered in detail in another article in this issue.)
NEOPLASMS
The opportunistic neoplasms Kaposi's sarcoma (KS) and non-Hodgkin's lymphoma involve the liver and spleen in approximately 15% of patients with AIDS. 17 They are seldom seen alone, but are usually part of multisystemic involvement. KS is an AIDS-defining illness and usually occurs early in the disease course. AIDS-related lymphoma (ARL) typically develops when there is profound imrnunosuppression (CD4 lymphocyte count < 50 ram3). TM Although many patients with AIDS have serological evidence of prior hepatitis B and C exposure, an increased incidence of hepatomas has not been reported. 18,19 Biliary obstruction due to ARL or KS usually results from extrinsic compression by enlarged lymph nodes or direct hepatic involvement. Primary biliary lymphoma or KS is rare.18,19 Renal cell carcinomas have been reported in patients with AIDS and have been attributed to the patient's immunodeficient state. Adenopathy resulting from ARL and KS can cause hydronephrosis.20-22
Kaposi's Sarcoma Kaposi's sarcoma is the most common neoplasm in patients with AIDS. This lesion is a purple nodule macroscopically that microscopically consists of irregularly dilated vascular spaces coated with swollen endothelial cells. 23Nearly one third of patients with cutaneous Kaposi's sarcoma will have hepatic involvement, but this is usually asymptomFrom the Department of Radiology, Northwestern University Medical School, Chicago, IL. Address reprint requests to Richard M. Gore, MD, Department of Radiology, Evanston Hospital, Northwestern University, 2650 Ridge Ave, Evanston, 1L 60201. Copyright © 1998 by W.B. Saunders Company 0887-2171/98/1902-000658. 00/0
Seminars in Ultrasound, CT, andMRI, Vo119, No 2 (April), 1998: pp 175-189
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176 Table 1. Hepatic and Splenic Parenchymal Diseases Associated With HIV Infection
Infection Bacterial Salmonella Rochalimaea Mycobacterial M tuberculosis M avium complex M xenopi Viral Cytomegalovirus Hepatitis B, C and D Herpesvirus Adenovirus HIV Fungal Candida Cryptococcus Histoplasma Aspergillus Coccidia Sporothrix Protozoal Pneumocystis Cryptosporidia Microsporidia Leishmania Toxoplasma
Neoplasms Non-Hodgkin's lymphoma Kaposi's sarcoma Metastatic cancer of the anal canal Drug-related Trimethoprim-sulfamethoxazole Ketoconazole Isoniazid Rifampin Zidovudine Pentamidine Diphenylhydantoin Prochlorperazine Didanosine Fluconazole Oxacillin Dideoxyinosine
atic and detected only at postmortem.24The diagnosis is usually made when cutaneous or nodal disease is discovered. Hepatic involvement typically causes only mildly elevated serum alkaline phosphatase levels.2 Detection of KS on imaging studies is difficult because the tumor spreads via microscopic perivascular infiltration. Although specific lesions are Table 2, Opportunistic Infections and Neoplasms Involving the Liver
% of Cases Infection Cytomegalovirus MAC Unspecified acid-fast bacilli Cryptococcus neoformans Histoplasma capsulatum Mycobacteria tuberculosis Candida albicans Neoplasms Kaposi's sarcoma Non-Hodgkin's lymphoma
14 11 5.9 2.0 1.2 1,2 0,6 8.6 1,5
Modified and reprinted by permission of the publisher from Bonacini M: Hepatobiliary Complications in Patients with Human Immunodeficiency Virus Infection. Am J Med 92:40441 I. Copyright 1997 by Excerpta Medica Inc.
Table 3. Renal Lesions Associated With HIV Infection
Disseminated infections Cytomegalovirus Mycobacterium tuberculosis Mycobacterium avium complex Cryptococcus Candida albicans Pneumocystis carinii Histoplasmosis HIV
Neoplasms Kaposi's sarcoma Lymphoma Renal cell carcinoma
Acute tubular necrosis Toxic Ischemic
Glomerular lesions Focal and segmental glomerulosclerosis (HIVassociated nephropathy) Mesangial proliferative glomerulonephritis Minimal change disease Membranoproliferative glomerulonephritis Membranous glomerulonephritis Acute postinfectious glomerulonephritis Vascular lesions Hemolytic-uremic syndrome Infarcts Renal cortical necrosis Vasculitis Allergic interstitial nephritis Drug-induced
rarely identified sonographically, hepatosplenomegaly may be present and small hyperechoic periportal and splenic nodules may be visualized causing increased periportal echogenicitye5 (Fig 1A). CT scans occasionally demonstrate low attenuation periportal lesions (Figs 1B, 2A) on noncontrast scans, which subsequently show enhancement on delayed, post-contrast scans. 25-28This finding is nonspecific. Distinctive CT features that indicate the diagnosis include the presence of normal or mildly enlarged lymph nodes that have high density approaching the attenuation of enhancing blood vessels due to the hypervascularity of the tumor26,27 (Fig 2B). They are usually observed in the groin but can be retroperitoneal, axillary, or pelvic in location.27 Skin nodules and nodular metastases to the hollow viscera and lung may also be seen. Renal involvement is usually microscopic and, consequently, found at autopsy rather than on imaging studies. If KS involves and enlarges the retroperitoneal lymph nodes, secondary obstructive uropathy may develop. 29,30
Lymphoma Non-Hodgkin's lymphoma is the second most common malignancy involving the liver, spleen, and kidneys in patients with AIDS.27 The frequency of non-Hodgkin's lymphoma is much higher in patients with AIDS than the general population and the disease course also differs. AIDS-related lym-
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phomas (ARLs) generally are B cell type centroblastic, lymphoblastic, or immunoblastic and are relatively aggressive, undifferentiated forms of lymphoma. 17 ARL tends to have a more advanced grade, greater extranodal disease, and a worse prognosis compared with lymphomas occurring in patients without AIDS. Their poor prognosis is also worsened by associated infections. On crosssectional imaging, ARLs present with hepatosplenomegaly, nephromegaly, and focal lesions. These lesions may vary in size and number: from a large isolated mass to innumerable tiny lesions (Fig 3). Focal lesions can also cause biliary dilatation. Focal hepatic lesions are observed much more commonly on ultrasound (45%) and CT (29%) in ARL when compared with the 5% to 10% incidence of focal abnormalities observed in sporadically occurring lymphoma. 31-34 Focal splenic le-
Fig 2. Kaposi's sarcoma in a 28-year-old man with AIDS. (A) CT scan demonstrates mesenteric and retroperitoneal lymphadenopathy with low density masses extending into the gastrohepatic ligament (black arrow) and portal veins (white open arrow). Hypodense splenic lesions (white arrow) are also identified. (B) This patient also has enlarged, contrastenhancing groin lymph nodes characteristic of adenopathy due to Kaposi's sarcoma (white arrows}.
sions are observed in 7% of AIDS patients and splenomegaly in 40% of cases. 31-34 Six to twelve percent of patients with ARL have renal involvement on imaging studies, which usually manifests as bilateral, discrete parenchymal masses (Fig 4), rather than the diffuse nephromegaly that typifies renal lymphoma in non-AIDS patients. Extensive retroperitoneal and/or mesenteric adenopathy is observed in 56% of ARL. 3~ These nodes usually have soft tissue density, but can occasionally show central necrosis. 35-37 They can also obstruct the renal collecting systems and ureters 37-39(Fig 5). INFECTIONS Fig 1. Kaposi's sarcoma in a 36-year-old man with AIDS. (A) Oblique sonogram demonstrates a periportal hyperechoic liver lesion (calipers) and echogenic periportal bands (arrows). Lymphoma and mycobacterial lesions of the liver tend to be hypoechoic while Kaposi's sarcoma lesions tend to be hyperechoic. (B) Post-contrast CT scan shows low attenuation periportal changes.
HIV infection causes progressive depletion of T-helper lymphocytes that play a pivotal role in the regulation of the immune system. As a result, AIDS patients are extraordinarily susceptible to opportunistic fungal, viral, protozoan, and mycobacterial
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infections.4° Unfortunately, these patients may reveal few systemic signs of infection and laboratory values may be misleading because there may be little fever or associated leukocytosis. Accordingly, cross-sectional imaging will occasionally reveal large abscesses that are clinically occult. Hepatic, splenic, biliary tract, pancreatic, and renal infections may develop during any stage of HIV disease, from the otherwise asymptomatic state to end-stage immunodeficiency. The specific organism infecting a given patient is determined by the degree o f immunosuppression. Most bacterial diseases, including Mycobacterium tuberculosis (MTB), are seen at early or intermediate stages of immunocompromise, when the CD4 lymphocyte count is 200 to 750 mm 3. Protozoan and fungal infections, such as cryptosporidiosis and Pneumocystis carinii (PC), occur when the CD4 lymphocyte count is less than 200 mm 3. Mycobacterium avium intracellular complex (MAC) and cytomegalovirus (CMV) infections almost always develop in the setting of profound immunosuppression (CD4 lymphocyte count < 60 mm3).4°
Fig 4. A 33-year-old woman with disseminated extranodal AIDS-related lymphoma. (A) Multiple low attenuation liver masses are identified (arrows). (B) Low attenuation renal lesions (black arrows) and retroperitonea! lymphadenopathy (open arrow) are seen. Renal biopsy demonstrated nonHodgkin's lymphoma in this patient.
Mycobacterium Avium Complex
Fig 3. A 42-year-old man with AIDS-related non-Hodgkin's lymphoma. (A) Multiple small hypodense liver masses are present. (B) Following chemotherapy, the liver lesions resolved.
Disseminated MAC infection is insidious, with a relatively late presentation, producing fever, anorexia, adenopathy, hepatosplenomegaly, and elevation of liver function tests.4~43 The most common abdominal sonographic and CT finding is lymphadenopathy44,45 (Fig 6). Radiological evidence of parenchymal involvement is often absent in spite of significant pathological involvement; focal lesions occur much more often in MTB than MAC. Perhaps the greater attenuation of the host immune status accounts for the absence of focal masses in MAC. Histologically, MAC causes multiple noncaseating grannlomas within the lobular parenchyma and portal tracts of the liver.46 MAC may present as multiple hypodense lesions on CT due to granuloma formation.4~ Sonographically, multiple tiny echogenic foci in the liver and
IMAGING OF ABDOMINAL AIDS
Fig 5. AIDS-related lymphoma in a 38-year-old man. (A) Retroperitoneal adenopathy and direct renal invasion causes hydronephrosis of the left kidney. (B) The left psoas muscle is also involved.
kidneys similar to extrapulmonary PC infection have been reported. 47,48Most commonly, however, only hepatosplenomegaly is observed on imaging studies. A high index of suspicion is required when processing biopsy specimens. They should be routinely stained for acid-fast bacilli and cultured for MAC, because caseating granulomatous reaction may be absent in patients with AIDS. 49 In the clinical setting of profound immunosuppression, the presumptive diagnosis of MAC can be made without biopsy if CT demonstrates focal hepatic, splenic, or renal (Fig 7) lesions associated with enlarged soft tissue density retroperitoneal or mesenteric lymph nodes (Fig 8) and focal jejunal thickening. 3°
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Fig 6. Hepatosplenomegaly associated with Mycobacterium avium complex. (A) CT scan shows mild hepatosplenomegaly associated with mesenteric and retroperitoneal lymphadenopathy. (B) A scan obtained several cm lower reveals adenopathy and focal mural thickening of the jejunum (arrow) and thickening of the gallbladder wall.
other evidence of AIDS and involve the liver, spleen, pancreas, and kidneys without pulmonary involvement.51 Less typical presentations are becoming more prevalent, and extrapulmonary in-
Mycobacterium Tuberculosis (MTB) After decades of decreasing incidence, a resurgence of MTB infection has accompanied the AIDS epidemic. 5° MTB infection may develop before
Fig 7. M),cobacterium avium complex renal abscess in a 40-year-old man with AIDS, Kaposi's sarcoma, and CMV infection of the esophagus, colon, and retina. Biopsy of this low density left renal mass demonstrated MAC.
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Fig 8. Retroperitoneal adenopathy associated with Mycobacterium avium complex. This organism was cultured after percutaneous biopsy of the 2 cm lymph node (arrow),
volvement is identified in up to 70% of AIDS patients with MTB including involvement of the liver, spleen, lymph nodes, central nervous system, bone, gastrointestinal tract, kidney, and soft tissues. 52 The liver is less commonly involved with MTB than MAC. Unlike MAC, MTB infection may occur before patients are significantly immunosuppressed. On CT, MTB presents with multifocal lesions in the liver, spleen (Fig 9), kidney (Fig 10), and pancreas often associated with enlarged, retroperitoneal and mesenteric lymph nodes that usually have central necrosis.41 Concomitant segmental ileocecal wall thickening may also be observed on CT. Hepatosplenomegaly is more impressive in MAC than in MTB. Low density lymph nodes are observed in 93% of patients with MTB but in only 14% of patients with MAC. 41
Fig 9. Mycobacterium tuberculosissplenic abscesses. Multiple hypodense lesions are seen within the spleen,
Fig 10. Mycobacterium tuberculosis renal abscess. (A) Longitudinal sonogram demonstrates an inhomogeneous mass (cursors) at the lower pole of the left kidney, (B) CT demonstrates a low density mass with a thick wall in the same region,
giF~ses
HIV infection is associated with disseminated hepatitis B and C viruses, CMV, herpes simplex virus, and Epstein-Barr virus due to similar modes of transmission. With acute hepatitis, sonography may demonstrate hepatomegaly associated with decreased liver echogenicity and prominent portal triads and mural thickening of the gallbladder. CT usually shows only hepatomegaly. Hepatitis B and C viruses can cause acute or chronic active hepatitis and ultimately postnecrotic cirrhosis. On crosssectional imaging, postnecrotic cirrhosis manifests as a nodular hepatic contour, enlargement of the caudate lobe and lateral segment of the left lobe, prominence of the fissures, regenerating nodules, and atrophy of the right and quadrate lobes. Sono-
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graphically, there is increased reflectivity of the fibrous tissue and a concomitant loss of definition of the portal vein walls associated with a generalized coarse, irregular, and heterogeneous echo architecture.53 CMV infection is common in patients with AIDS, seen in up to two thirds of autopsies. CMV may affect any part of the GI tract, generally presenting with ulcers of the esophagus, stomach, and/or colon, s4,55 Hepatic, renal, and pancreatic involvement is observed less frequently. Coinfection with cryptosporidium and Candida albicans is common. CMV involves the liver in up to 44% of AIDS patients at autopsy, but generally is clinically silent unlike biliary, gastrointestinal, or pulmonary infection)4,55 CMV infection may manifest with multiple echogenic liver lesions sonographically and multiple low attenuation lesions on CT (Fig 11). Hepatic or renal infection by CMV does not significantly alter patient prognosis) 6
Bacterial Abscesses All AIDS patients, but particularly those who are intravenous drug abusers, are prone to develop septic emboli and abscesses from a variety of bacteria, most often Staphylococcus aureus. The lungs, liver, spleen (Fig 12), and kidneys (Fig 13) may also be involved due to hematogenous disseminationY ,58 Multiple organisms are often cultured from these abscesses.
Fungal Infections The liver and spleen are often infected in AIDS patients with disseminated Candida albicans, 59 Cryptococcus neoformans, HistopIasma capsularum, and Coccidioides immitis organisms. Candidiasis can cause hepatic, splenic (Fig 14), pancreatic, and renal microabscesses, especially in intravenous drug abusers. The diagnosis of candidiasis can be difficult because the clinical and radiological presentation is nonspecific, and this organism may be difficult to culture following biopsy.59,6° Additionally, blood cultures are positive in only 50% of patients. Candida microabscesses typically appear as multiple small hypoechoic lesions on sonography or hypodense lesions on CT scans, best seen following intravenous contrast material injection. 6°,61
Pneumocystis Carinii Extrapulmonary PC infection is occurring more frequently in AIDS patients due to their longer life
Fig 11. Focal hepatic lesions associated with CMV infection. (A) CT shows multiple hypodense liver masses. (B) These lesions are echogenic on ultrasound,
span and the introduction of prophylactic aerosolized pentamidine.62 Although therapy produces drug levels sufficient to prevent pulmonary infection, systemic distribution is inadequate, encouraging extrapulmonic disease spread to the liver, spleen, kidneys, lymph nodes, bone marrow and, less often, to the adrenal glands, retina, thyroid and parathyroid glands, gallbladder, and pancreas. Pneumocystis carinii pneumonia spreads both hematogeneously and lymphogeneously. Fortunately, extrapulmonic spread occurs in fewer than 1% of patients. Disseminated disease is usually a premorbid event unless systemic treatment is provided, only a solitary extrapulmonary site is involved, or if there is no concurrent active pulmonary infection. Sonography of the liver, spleen, and kidneys
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Fig 12. Pyogenic and protozoan abscesses in a 34-year-old febrile man with AIDS and splenic abscesses, CT demonstrates several hypodense splenic lesions one of which has peripheral calcification. Percutaneous aspiration revealed Pneumocystis carinii, Klebsiella, and E coli,
may show small hypoechoic masses or multiple tiny echogenic foci without shadowing 62-64 (Fig 15). The echogenic loci are due to calcifications or granulomas. CT scans may demonstrate hypodense lesions or calcifications of the liver, spleen and kidneys 62-65 (Fig 16). Associated findings include punctate calcifications of the adrenal glands and lymph nodes. A history of PC pneumonia, aerosolized pentamidine prophylaxis, and progressive calcification of the liver, spleen, and other organs is suggestive of extrapulmonary PC infection.62Calcifications within these lesions do not necessarily signify healed, inactive disease as they do in candidiasis and lymphoma. These calcifications were initially believed to be pathognomonic for pneumocystis infection, but have recently been
Fig 13. Bilateral wedge-shaped infarcts due to septic emboll are seen in the kidneys of this AIDS patient with E coil septicemia. Note the splenomegaly,
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Fig 14. Candidiasis in a 33-year-old intravenous drug abuser with AIDS. Splenic involvement manifests as multiple small low attenuation lesions.
described in MAC and cytomegalovirus infection.66,67 AIDS-RELATED CHOLANGITIS
Although hepatic parenchymal involvement with opportunistic infection and malignancy has been well described, the biliary tract sequelae of HIV infection are less well appreciated. Four different patterns of HIV-related cholangiopathy have been reported: 1. Papillary stenosis in which there is dilatation of bile ducts and delayed drainage of contrast into the duodenum. 2. Sclerosing cholangitis characterized by focal strictures and dilatations of the intra- and/or extrahepatic bile ducts. 3. Combined papillary stenosis and intra- and/or extrahepatic sclerosing cholangitis. 4. Long extrahepatic bile duct strictures with lengths exceeding 1 to 2 cm. Biliary tract infections by several organisms, but especially CMV and cryptosporidium, have been implicated in the development of AIDS-related cholangitis but not directly demonstrated as cansative. 2,68,69Other associated infections include MAC, Microsporidium, and Isospora. 58,7° Direct involvement by HIV infection has also been postulated as causative. CMV-associated acalculous cholecystitis has been described, but does not appear to be associated with HIV cholangiopathy, as the two are rarely observed in the same patient. 71 Pathologically, there is inflammation and edema of the gallbladder wall and mucosal ulceration. CMV inclusion bodies characteristically are located near mucosal ulcers.
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Fig 15. AIDS-related Pneumocystis carinfi infection in a 27-year-old man with prior Pneurnocystis infections who had received prophylactic aerosolized pentamidine. (A) Longitudinal sonogram demonstrates multiple tiny echogenic foci in the liver and right kidney, (B) Multiple tiny echogenic foci are also present on this longitudinal scan of the spleen. (C) Corresponding CT reveals multiple calcifications in the spleen and gastrohepatic ligament, Calcifications are typical of Pneumocystis infection and may be present in both active and resolved infections.
Cryptosporidiosis infection is present in 6% of all AIDS patients and 21% of those with diarrhea. 72 The identification of biliary cryptosporidium is difficult; currently, there is no effective therapy for the irradiation of this organism. 59,73 Ultrasound, CT scans (Figs 17 through 19), and ERCP are complementary in the diagnosis of AIDS-related cholangiopathy. 74-%Ultrasound findings include dilatation and mural thickening of the gallbladder and common bile ducts as well as pericholecystic fluid. Dilated intrahepatic ducts are
often observed. 74,78 An echogenic nodule may be seen at the distal end of the common bile duct representing an edematous papilla of Vater. Gallbladder dilatation and sludge are also commonly found in AIDS patients. On CT, inflammation of the gallbladder or biliary tree is manifested by mural thickening and/or abnormal contrast enhancement. The cholangiographic signs of beading, pruning, and nodular mural thickening can also be observed. Patients with AIDS often have asymptomatic gallbladder wall thickening that does not
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require treatment. The exact cause is unknown and may relate to hepatic dysfunction, hepatitis, hypoproteinemia, or opportunistic infections (typically CMV and cryptosporidium) that may induce acalculous cholecystitis. Reversible symptomatic gallbladder wall thickening has been described during infusion of interleukin-2 therapy. 74-v9 Cholangiography is more sensitive and specific than ultrasound and CT in depicting the shagginess and mural irregularity of the extrahepatic ducts that result from exuberant periductal inflammation, focal mucosal ulcers, and interstitial edema found in AIDS-related cholangitis. In addition, therapeutic procedures such as sphincterotomy, especially in patients with papillary stenosis, may provide temporary symptomatic relief. However, ERCP is invasive and can cause pancreatitis.
Fig 17. Mural thickening of the gallbladder in a 43-year-old AIDS patient with elevated liver function tests and Cryptosporidiurn infection. (A) Longitudinal sonogram shows marked mural thickening of the gallbladder (arrows). (B) CT scan shows low density wall thickening with enhancing mucosa causing "pseudogallstone" appearance (arrow). Note the periportal lucency, which is usually caused by secondary periportal edema related to lymphadenitis, hepatitis, or malnutrition. Mild retroperitoneal adenopathy is also seen.
PARENCHYMAL LIVER DISEASE
Fig 16. Extrapulmonary Pneumocystis carinfi infection. (A) Transverse sonogram demonstrates echogenic reflectors in the right kidney secondary to calcifications. (B) Non-contrast CT scan shows multiple renal calcifications. When extrapulmonary Pneumocystis is suspected, non-contrast images should be obtained.
A wide variety of disorders (Tables 1, 2) associated with HIV infection and AIDS can affect the liver. Although most of these represent opportunistic infections, ARL, KS, and hepatocellular injury from drugs used in the treatment of AIDS also must be considered. Additionally, there may be coexisting liver disease unrelated to HIV infection such as chronic viral hepatitis or liver injury from alcohol or drug abuse. Serological markers for concurrent hepatitis B virus infection are present in 90% of patients with AIDS. This concurrent infection does not appear to alter the natural history of HIV infection. Hepatic steatosis is a common postmortem find-
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ing in patients with AIDS. s° The pathogenesis of fatty change is complex and relates to the effects of circulating cytokines such as tumor necrosis factor, interleukin- 1, and interferons.Sl Focal fatty infiltration can mimic other mass lesions. Imaging findings of hepatic steatosis are similar to those found in non-AIDS patients. 53 On CT, there are diffuse, focal, segmental, or geographic areas of low attenuation in the liver. Sonographically, involved areas show accentuation of echogenic foci resulting from the proliferation of fat-nonfat interfaces. This leads to rapid attenuation of the insonating ultrasound beam. A diffusely echogenic liver can also result from multiple granulomata secondary to infections such as MAC, MTB, cryptococcosis, histoplasmosis, and toxoplasmosis. 82-85Drug toxicity may manifest as hepatic steatosis or as multiple granulomas that also cause an echogenic liver on sonography, sl Bacillary peliosis hepatitis is a recently recog-
Fig 19. Cryptosporidiosis of the bile ducts and small bowel in an HIV-positive 22-year-old man with diarrhea and elevated liver enzyme levels. (A) CT scan shows dilated intrahepatic ducts that have thick enhancing walls. (B) More caudal scan shows mural thickening of the small bowel,
Fig 18. AIDS-induced papillary stenosis due to cryptosporidiosis in a 33-year-old man. (A) Oblique sonogram demonstrates dilatation of the common hepatic duct and mural thickening of the gallbladder {arrows), (B) Transverse sonogram of the pancreas shows dilatation of the common bile duct (large arrow) and pancreatic duct (small arrow),
nized complication of AIDS, found in patients with CD4 lymphocyte counts < 200 per mm 3. It is caused by systemic infection by either Rochalimaea henselae or Rochalimaea quintana, two newly recognized bacteria related to Bartonella species, of the Rickettsiae order. This disorder is associated with cutaneous angiomatous lesions and lytic bone lesions and clinically manifests with fever, chills, sweats, bone pain, and abdominal or right upper quadrant pain. Pathologically, there are dilated vascular lakes that are associated with proliferation of sinusoidal endothelial cells, blebbing of hepatocyte membranes, extravasation of red blood cells, and dilatation of Disse's spaces. 86 The CT findings vary based on the size of the vascular cavities. Small cavities are not visible on cross-sectional imaging studies, whereas larger cavities may have an attenuation similar to blood vessels or appear as hypodense defects. Complications such as liver failure, portal hypertension, and
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hemorrhage from hepatic or splenic rupture may develop, s6.Ss PANCREATIC DISEASES
Pancreatic diseases, although commonly detected at autopsy, often are not recognized during life but can be a source of morbidity in patients with AIDS. 7~ These patients are subject to a variety of pancreatic disorders in addition to those seen in the general population: opportunistic infections, drug-induced inflammation, and neoplasms, s9 Involvement can range from asymptomatic findings detected at autopsy to fulminant pancreatitis leading to death. Gross pathological changes vary from a normal pancreas in some infections and tumors to massive necrosis and abscess formation. Special stains for fungi and mycobacteria and detection of viral inclusions are required for diagnosis following biopsy. Generally, the patients are asymptomatic with involvement of other organs by infections or neoplasms. 9° Reported opportunistic infections that affect the pancreas include CMV (Fig 20), MAC, MTB, Cryptococcus neoformans, Aspergillosis, and candidiasis. 55 Extrapulmonary PC rarely involves the pancreas and may be seen as tiny echogenic foci on ultrasound or calcifications on CT examination. 91 Medications including pentamidine and trimethoprim-sulfamethoxazole, both used to treat PC pneumonia, can cause pancreatitis indistinguishable from other causes. There is a 7% prevalence rate of pancreatic neoplasms in AIDS patients at autopsy, most commonly, Kaposi's sarcoma and lymphoma. The involvement appears to be subclinical and usually is associated with disseminated disease. The radiographic features of pancreatitis and pancreatic abscesses in patients with AIDS are similar to that of the general population. Two caveats should be remembered when using ultrasound. When comparing pancreatic to hepatic parenchymal echogenicity, it should be remembered that the liver is often echogenic in patients with AIDS due to fatty infiltration, so that the normal pancreas may appear relatively hypoechoic, simulating pancreatitis. 53 Similarly, the kidney is not always a reliable internal reference; the parenchyma may be hyperechoic due to HIV-associated nephropathy. HIV NEPHROPATHY
HIV-associated nephropathy can develop in patients with asymptomatic HIV infection, AIDS-
Fig 20. Cytomegalovirus pancreatitis with pseudocysts in a 33-year-old man with AIDS. (A and B) This AIDS patient had a history of complicated pancreatitis with recurrent pseudocysts (P) noted on sonography and CT scan that required drainage. Pancreatic biopsy confirmed characteristic CMV inclusion bodies.
related complex, or AIDS.92 Patients typically have mild hypertension, large kidneys with early and rapidly progressive renal failure with massive proteinuria, hematuria, and azotemia. 93 Renal involvement is more prevalent in AIDS patients with multiple risk factors and intravenous drug abuse than the homosexual population with AIDS. 94,95 The disease is most commonly seen in black males and has an inexorably downhill course with 100% mortality within 6 months after the onset of uremia despite hemodialysis. Focal and segmental glomeru-
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cortical e c h o g e n i c i t y (Fig 21), w h i c h is m o s t likely the result o f the g l o m e r u l o s c l e r o s i s and the dilated renal tubules filled with proteinaceous material. H o w e v e r , a direct correlation b e t w e e n the extent o f renal disease and d e g r e e of e c h o g e n i c i t y does not exist.96, 97 The m a j o r C T findings in H I V nephropathy include n e p h r o m e g a l y due to p a r e n c h y m a l inflammation and edema, increased attenuation o f the m e d u l l a on non-contrast scans, and a striated n e p h r o g r a m f o l l o w i n g contrast administration due to the dilated tubules filled with proteinaceous material. 9~ SUMMARY Fig 21. A 24-year-old male with HIV nephropathy, Longitudinal sonogram demonstrates an enlarged right kidney with increased cortical echogenicity.
losclerosis are the histopathologic hallmarks o f H I V - a s s o c i a t e d nephropathy. T h e r e is m i c r o c y s t i c dilatation o f renal tubules, with the l u m e n filled with pale-staining casts and n u m e r o u s protein absorption droplets. T h e sonographic correlates o f this p a t h o l o g y are n e p h r o m e g a l y and increased
Hepatic, splenic, biliary tract, pancreatic, and renal c o n s e q u e n c e s o f H I V disease are diverse. S o m e are unique and specifically attributable to H I V infection, whereas others are coincidental, reflecting the nature and severity o f the underlying primary illness. As patients with A I D S are living longer, solid a b d o m i n a l visceral i n v o l v e m e n t is b e c o m i n g m o r e c o m m o n , and an understanding o f the s p e c t r u m o f H I V - a s s o c i a t e d disease is essential for i m p r o v i n g patient m a n a g e m e n t . 99
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